Term
| What are the 2 division of the Peripheral Nervous system? |
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Definition
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Term
| Where does the afferent pathway lead to in the CNS and what type of neurons does it carry? Efferent? |
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Definition
1) Afferent pathway go TOWARDS the CNS and has sensory neurons (have cell bodies)
2) Efferent pathway goes AWAY for the CNA and has motor neurons |
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Term
| What are the 2 divergences of the Afferent pathway? |
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Definition
| 1) Somatic 2) Visceral (part of ANS) |
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Term
What are the 2 divergences of the Efferent pathway?
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Definition
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Term
| What does the efferent somatic neuron innervate and what type of neuron is it? |
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Definition
1) Skeletal muscle 2)Motor neurons
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Term
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Definition
| Motor neurons and all the fibers that it innervates? |
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Term
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Definition
| Where the motor neuron synapses with the muscle fibers |
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Term
| Would you consider the back muslces or the finger muscles to have more synapses with motor neurons? Why? |
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Definition
| The finger muscles becuase they need them for fine control vs. back do not need that many |
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Term
| What is diffrent between a NMJ and a regular somatic junction? |
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Definition
| At the NMJ the Ach Receptors are grouped at the muscle folds. |
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Term
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Definition
| Neuromuscular Junction is where the motor neuron meets the muscle fiber |
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Term
| At the NMJ when the Ach receptors are stimulated what happens? |
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Definition
| Stimulation leads to change in the membran potential (of the muscle fiber) causing an END PLATE POTENTIAL |
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Term
| Compare an EPP (end plate potential) to an EPSp? |
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Definition
| EPP happens in muscle fibers and usually one EPP is good enough to cause an action potential (Doesnt need to summate) and EPSP happens in neurons and usually the EPSP's have to summate inorder to cause an AP. |
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Term
| What are the disadvantages of having an EPP that usually always causes an AP? |
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Definition
| Will constantly contract upon release of Ach, thus hard to control the skeletal muscle |
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Term
| How do you control skeletal muscle? |
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Definition
| By how many motor units you recruite or activate. The more motor neurons you recruite the more increase muscle contraction you will have. |
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Term
| What ion flow into the muscle fiber once the Ach receptor is activated? |
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Definition
| Na+ to depolarize the cell. |
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Term
| Once an EPP is intiated ( by motor neuron) and action potential is made where the the AP spread on the muscle fiber? |
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Definition
| Sarcolemma and Transverse tubule (T-tubule) |
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Term
| What type of voltage gated channels can be found on the T-tubule membrane? |
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Definition
| DHPR (voltage gated Ca+2 channels) |
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Term
| What happens after the AP (Caused by the EPP in skeletal muscle) travels down the sarcolemma and the T-tubule? |
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Definition
| The AP opens/activates the VG Ca2+ channels (DHPR) and induces release of intracellular Ca+2 from Sarcoplasmic Reticulum (SR) |
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Term
| Write out the steps for excitation contraction coupling? |
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Definition
| 1) Ach binds to Nicotinic receptors 2) Na+ goes down its concentration gradient causing depolarization thus causing an EPP which usually always causes an AP 3) AP spreads down the sarcolemma and T-tubule 4) Activates the DHPR's 5) DHPR's activates the Ryanodine receptor 6) Ca+2 flows out of the SR 7) Ca+2 binds to Troponin (on Actin filament) on region TnC 8) Tropomyosin moves and exposes the actin binding sites and myosin head attaches to the actin site and move actin toward the center causing muscle contraction. |
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Term
| Describe the skeletal muscle organization? |
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Definition
| Muscle-->muscle fibers--> Muscle fiber--> Myofibril --> Sarcomere |
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Term
| What is the Sarcomere comprised of? |
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Definition
| Z-line, Actine, Myosin, tropomyosin, troponin.... |
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Term
| What holds the sarcomere in place? |
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Definition
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Term
| Describe A-band, I-band, H-band, Z-line, M-line and what happens to them during contraction of the sarcomere? |
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Definition
1) A-band:Length of the myosin/thick bands. Does not change during contraction.
2) I-Band: Where the thin filaments (Actin) with no overlap with Myosin. It decreases during contraction.
3)H-Band: Only thick filament where there is no thin filament. Decreases during contraction
4) Z-line:
A dark thin protein band to which actin filaments are attached in a striated muscle fiber, marking the boundaries between adjacent sarcomeres. No change during contraction.
5) M-line: Dark band in center, no change during contraction.
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Term
| T/F: Myosin length can be changed |
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Definition
| False; Myosin length canNOT be changed. |
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Term
| What does a myosin filament have that allows it to move the actin fillaments? |
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Definition
| Myosin heads (binds to actin) |
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Term
| How many varaiations fo heads does the myosin filament have? and What are their fxn when comparing fast twitch and slow twitch? |
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Definition
| 1) Heavy chain (S1) 2) Light chain (Alkali) |
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Term
| Define each 1) Actin 2) Tropomysin 3) Troponin |
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Definition
1) Actiin- aka Thin Filament, has bindng site where myosin binds when contracting
2) Tropomyosin- String like that covers the actin binding sites with the aid of troponin
3) Troponin- Blocks the tropomyosin from being removed from the active site. Has three components |
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Term
| What are the 3 components of Troponin? |
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Definition
1) TnT- Binds to troponin
2) TnC- Binds to calcium
3) TnI- Binds to actin (to keep Tropomysoin and actin in place) |
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Term
| Where specifically does tropomyosin bind to cause a shift in tropomyosin? |
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Definition
| Troponin-C (in the troponin complex) |
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Term
| T/F: One of Myosin's fxn is to hydrolyze ATP. |
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Definition
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Term
| When does myosin detaches from actin? |
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Definition
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Term
| Write step-by step process of hydrolysis of ATP and the powerstorke? |
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Definition
1) Released state: ATP binds to myosin head causing the dissociation of the actin-myosin complex
2)Cocked State: ATP is hydrolyzed causing myosin head to return to their resting state.
3) Cross-bridge state: A cross-bridge forms and the myosin head binds to a new position on actin.
4)Power Stroke state: Phosphate is relased, Myosin head changes conformation resulting in the power stroke. The filaments slide past each other (actin filament moves toward the middle)
5) Attached state: ADP is released |
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Term
| What does the Huxley sliding filament theory state? |
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Definition
| Theory of how muscles contract; actin and myosin interact and actin sliding over myosin and sarcomere getting shorter thus creating a contraction. |
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Term
| What happens when the contraction is gong to be stopped? (3 Steps) |
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Definition
| Ach is brokendown, then synthesized, and packaged againg for reuse. |
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Term
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Definition
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Term
| What are the by-products of AchE hydrolyzing Ach? |
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Definition
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Term
| From AchE byproducts which byproduct is sent back to pre-synaptic? and how does it get back in? |
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Definition
| - Choline is sent back into pre-synaptic end of the neuron via Choline transporter |
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Term
| What type of transporter is the choline transporter? |
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Definition
| Secondary active co-transport |
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Term
| Once choline is inside the pre-synaptic neuron how does it go to be packaged into a vesicle? |
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Definition
| 1) Choline and acetyl CoA make Ach via the enzyme CHaT 2) Ach Transporter packs Ach into the vesicle |
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Term
| What type of transporter aids in putting Ach back into the vesicle? |
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Definition
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Term
| What are 2 important things you need to terminate contraction of the muscles? |
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Definition
| 1) Acetylcholinesterase 2) Re-up take of Ca+2 |
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Term
| What 3 things need to be active inorder to take up Ca+2 (during termination of contraction)? |
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Definition
1) NCX- moves Ca+2 out of muscle fiber (using gradient of Na+) moving Na+ out.
2) SERCA- on SR to pump Ca+2 and against its conc. gradient
3) Calsequestrin- Helps hold the Ca+2 in the SR |
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Term
| After NCX is done pumping Ca+ out, what is used to restore the ionic concentration (since NCX uses Na+ (going down its gradient)? |
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Definition
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Term
| What 5 factors is an indication of muscle fatigue? |
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Definition
1) ATP depletion 2) Na/K ionic imbalance ( not enought Na+ outside muscle to flow down nicotinic receptors)
3) lactic acid and Phosphate (from ATP myosin hydrolysis) accumalation
4) Inhibition of SR calcium release and Reuptake
5) Glycogen depletion (ATP source) |
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Term
| Patients with mailgnant hyperthermia (from being adminstered Sux) have a mutation in what receptor? And what is the effect of the mutation? |
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Definition
| Ryanodine receptor (RYR1) or voltage gated Ca+2 channels. Causes excess uncontrolled flow of Ca+2 out of SR causing Drastic and uncontrolled increase in skeletal muscle oxidative metabolism. Causes Inc. HR, Dec. BP, Inc. Temp, O2 debt, Inc. in pCO2 (which causes Inc. metabolic and respiratory acidosis |
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Term
| What is the treatment of Malignant hypothermia caused by sux? Its mechanism? |
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Definition
| Dantrolene- Blocks Ca+2 release channels in skeletal muscle- by blocking ryanodine receptors. it basically reduces metobalism of Ca+2 |
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Term
| What type of protein is found in striated muscle(Heart and Skeletal)? |
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Definition
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Term
| What is the difference between myoglobin and hemeglobin? |
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Definition
| Myoglobin binds to O2 with a higher affinity |
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Term
| Why is myoglobin specifically in O2 muscle cells? |
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Definition
| Help increase O2 in muscle cells |
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Term
| T/F: Myoglobin binds to about the same amount of oxygen as Hemeglobin but binds to oxygen at a lower pressure= thus increasing the affinity to oxygen |
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Definition
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Term
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Definition
| Break down of muscle fibers |
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Term
| Why does Rhabdomyolysis occur? |
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Definition
| Release of myoglobin (from broken down muscle fibers) filtered by kidneys (which causes damage) |
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Term
| What 3 things cause rabdomyolysis? |
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Definition
1) Extreme exertion
2) Extreme shaking with chills (when your cold)
3) Trauma to muscles
4) Malignant hypothermia |
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Term
| What are the symptoms of Rabdomyolysis? |
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Definition
1) Red urine
2) Muscle pain/weakness/fatigue |
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Term
| Does rhabdomyolysis Inc. or Dec. 1) Creatine Kinase 2) Potassium 3)Myoglobin in the blood? |
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Definition
| A blood serum of a patient encountering rhabdomyolysis usually will have High creatine kinase, potassium, myoglobin |
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Term
| Name 5 things you can block to block synaptic transmission for skeletal muscle contraction and name the drugs that do so. |
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Definition
1) VG Na+ (on axon)- Tetradoxin, Lidocaine
2) VG Ca+2 channels (on presynaptic terminal)-w-conotoxin
3) Ach Release- Tetanus toxin and botulism toxin
4) AchE- Nerve gas, Physostigmine
5) AchR (nicotinic channel)- Sux, Tubocurarine |
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Term
| What drug blocks Ca+ channels (on presynaptic cell) |
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Definition
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Term
| What drugs block VG Na+ channels? |
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Definition
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Term
| What 2 drugs block Ach release |
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Definition
| Botulism toxin, and tetanus toxin |
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Term
| What type of drug blocks AchE (acetylcholinesterase) |
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Definition
| Physostigmine and Nerve gas |
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Term
| What type of drugs block AchR release? |
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Definition
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Term
| How does Succinly choline chloride relate to Acetylcholine? |
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Definition
| Sux is two Ach joine together |
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Term
| What effect does Sux have on the cell membrane |
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Definition
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Term
| What is Sux a partial agonist for? |
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Definition
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Term
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Definition
It chronicly activates AchR and maintains depolarization and PREVENTS OTHER AP's thus causing paralysis
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Term
| T/F: Sux causes depolarizations but prevents repolarizations |
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Definition
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Term
| How is a d-tubocurarine differ from Sux? |
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Definition
| D-Tubocurarine is a non-depolarizing muscle relaxant and Sux is a depolarizing muscle relaxant. D- Tubocur' acts as a antagonist to the AchR receptor so the cell doesn't even depolarize at all.Vs. Sux acts as a agonist to the AchR but keeps it open to deactivate it. |
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Term
| What are 2 things Myasthenia Gravis caused by? |
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Definition
1) Autoimmune disease
2)Antibody production to Ach nicotinic receptors |
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Term
| What are symptoms of myasthenia gravis? |
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Definition
| Weakening of skeletal muscles |
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Term
| if a Patient with Myasthenia gravis has an EPP, will it usually cause an AP? |
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Definition
| No, becuase MG patients have low AchR to pick up the signal. |
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Term
| What is the turnover rate of AchR in a normal patient vs. a Myasenthia gravis patient? |
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Definition
| Normal patient has a longer (5-7 day) turnover rate than MG (2-3 days) |
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Term
| Will Sux work on MG patients? |
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Definition
| Yes, MG patients still have AchR receptors, but the effect will not be as much amplified, since the lack of AchR receptors. |
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